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Christopher E. Ramsden, Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, USA;
Many patients with chronic pain continue to experience substantial pain and impaired quality of life despite taking numerous pain-related medications. It is therefore essential to investigate novel mechanisms and alternative approaches to manage pain. As major components of immune, myelin, glial, and neuronal cell membranes, n-3 and n-6 fatty acids can be endogenously converted to several families of bioactive lipid autacoids with pro- or antinociceptive properties (eg, endovanilloids, eicosanoids, endocannabinoids, resolvins). With a few notable exceptions, mediators derived from n-6 linoleic (LA) and arachidonic (AA) promote nociception, while mediators derived from n-3 eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) promote anti-nociception. Thus, an imbalance of mediators derived from n-3 and n-6 fatty acids is a plausible mechanism underlying initiation and perpetuation of chronic pain disorders including headaches. In a small randomized trial in 67 patients with chronic headaches, we found that increasing dietary n-3 with concurrent reduction in n-6 fatty acids (the H3-L6 diet) produced statistically significant reductions in headache frequency and severity. These clinical improvements were accompanied by increases in pathway precursors for n-3 derived lipid mediators of anti-nociception, and reductions in n-6 derived mediators of nociception in circulation. Therefore, targeted alterations in dietary n-6 and n-3 fatty acids may be able to modulate nociceptive lipid mediators to reduce physical pain. However, current understanding of the molecular pathways and specific lipid autacoids linking diet to physical pain is limited. In this presentation I will review emerging preclinical and clinical evidence and highlight key evidence gaps along the proposed causal chain linking dietary n-3 and n-6 fatty acids to the etiology of chronic pain.